Parvovirus infection is responsible for erythema infectiosum (Fifth's disease) in children and aplastic crisis, hemolytic anemias, and fetal death, as well as a rheumatic syndrome in adults. It is also reported to be responsible for anemias, fevers, pneumonitis, and aplastic crisis in AIDS patients. The human B19 parvovirus is most commonly implicated. Little is known about B19 due to its difficult in vitro propagation. A simian counterpart to this human virus was previously isolated elsewhere from a cynomolgus monkey with anemia. We recently showed histologic evidence in the bone marrow of a severely anemic rhesus monkey with advanced SIV immunodeficiency disease, suggesting parvovirus infection in this species as well. Bone marrow and other tissues from this animal were collected and cryopreserved. We conducted a pilot experiment where bone marrow from the sentinal animal was inoculated by the intravenous route into six animals (three naive, and three SIV infected) to determine whether we could reisolate virus as well as reproduce the disease, and whether immunodeficiency was a requirement for disease. We developed a molecular PCR assay for diagnosis of infection. Five of six animals were infected. Virus appeared in the peripheral circulation by day four, peaked by day 11, and was below the level of detection by day 14 post inoculation (p.i.). There was no more evidence of infection, until 5 week p.i., when one animal again was PCR +. Virus shedding continued for two more months until the animal was humanely euthanized. Three other animals have also progressed to disease and died. Two of these animals produced severe anemia with a very significant drop in their peripheral hematocrit and hemoglobin levels. A third animal demonstrated a less significant drop in those same values. The fourth animal had no suggestion of anemia, however, died due to complication of SIV disease. Two final animals remain alive and are virus free. All anemic animals were positive for virus at the time of necropsy, suggesting that the rhesus parvovirus is responsible for the anemia observed. Our hypotheses that immunodeficient animals would more readily progress to disease and that SIV is a cofactor of disease, is still possible, however, not clearly answered. The two of the three previously SIV infected animals all remain alive suggesting those animals were not severely immunodeficient at the time of Parvovirus inoculation, and they were probably were resistant to superinfection with the second SIV strain in the bone marrow inoculum. All three naive animals in the other group progressed to disease and died. They all showed classic signs of SIV immunodeficiency following their coinoculation of SIV and Parvovirus. We are